AR and cancer: Although multiple docetaxel resistance mechanisms have been revealed through extensive research, such as upregulation of drug efflux pumps (e.g. ABCB1) (40), alterations to β-tubulin and expression of tubulin isoforms (41), deregulation of apoptosis and survival signalling pathways (42), induction of EMT and cancer stem cells phenotypes (36, 43, 44), and deregulation of AR signalling (45), the development of clinically useful tools to predict response is currently still required (46–48).